Acutepoisoning guidelinesforinitialmanagement-130630080645-phpapp02

ACUTE POISONING
GUIDELINES FOR INITIAL
MANAGEMENT
Prof. Dr. Saad S Al Ani

Senior Pediatric Consultant
Head of Pediatric Department
Khorfakkan Hospital
Sharjah ,UAE
saadsalani@yahoo.com

INTRODUCTION
• The majority of poisonings are
accidental, especially in the under-5
age group
• Intentional overdoses and substance
abuse are seen in older children
http://emedicine.medscape.com/pediatrics_general/

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CONT.
•

•

Deaths in children from poisoning are
becoming increasingly rare
Factors responsible for this decline
include:
1. Introduction of child-resistant
containers
2. Reducing the pack sizes of aspirin and
acetaminophen
3. More effective management

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HOW CHILDREN DIFFER FROM ADULTS
•

•

Pediatric patients may be particularly
vulnerable to certain toxins at specific
stages of childhood.
Breast fed infants may be exposed to
drugs or toxins excreted in breast milk;
neonates have immature metabolic
capabilities

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CONT.
• Toddlers, as they develop exploratory
hand-to-mouth activity, may be
exposed to a wide range of potential
hazards

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GENERAL PRINCIPLES
Assess:
 Type

of ingestion (drug, preparation)
 Time of incident
 Amount of ingestion (include all medication
that was potentially in the bottle or packet
when calculating)
 Weight of child
http://www.rch.org.au/clinicalguide/guideline_index/Acute_Poisoning_Guidelines_For_Initial_
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GENERAL PRINCIPLES
Cont.
 Is the ingestion potentially harmful?
 Beware of the possibility of mixed overdose
 Beware of the possibility of inaccurate dose
reporting on history taking
 If mixed or undetermined ingestion
Paracetamol level should be done
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GENERAL PRINCIPLES
Management
 Airway
 Breathing
 Circulation
 Removal of poison (if necessary)
 Emesis
 No role in the hospital setting
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GENERAL PRINCIPLES
Cont.


Activated Charcoal
The treatment of choice for most ingestions.
Most effective when given within first hour.

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GENERAL PRINCIPLES
Cont.
Activated Charcoal Contraindications:
•Patients with altered conscious state
•The following agents:
1.Ethanol/glycols

6.Potassium and other metallic ions

2.Alkalis

7.Fluoride

3.Boric acid

8.Cyanide

4.Lithium

9.Hydrocarbons

5.Iron compounds

10.Mineral acids

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GENERAL PRINCIPLES
Cont.
Whole Bowel Irrigation has a limited role
in treatment of some slow release
preparations
 Gastric Lavage has a very limited role in
treatment and should not be used without
consultation.
 Specific antidotes may be available and
serum drug levels may help in treatment
decisions


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GENERAL PRINCIPLES

Cont.
All acts of deliberate self harm must be
taken extremely seriously.
 All intentional self poisonings in
adolescents require admission
 If unexplained symptoms exist a urinary
drug screen may be indicated


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INITIAL ASSESSMENT AND MANAGEMENT

The

initial priority in treating poisoned
children is the standard ABC
(airway, breathing, and circulation)
resuscitation approach

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A: ASSESS AIRWAY PATENCY
By

looking, listening, and feeling for
air movement.
 If there is no air movement, try to open
the airway with simple maneuvers such
as the jaw thrust or the use of airway
adjuncts.

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CONT.
Certain

ingested agents may predispose
to airway edema and
obstruction, including caustic
agents, angiotensin-converting enzyme
inhibitors, and plants containing
calcium oxalate crystals
(e.g. Dieffenbachia and
Philodendron house plants)

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B: ASSESS THE ADEQUACY OF BREATHING

It is important to remember that
succinylcholine may cause prolonged
block in children who have a reduced
cholinesterase concentration due to
exposure to cocaine or
organophosphate compounds:
prolonged apneas of up to 7 h have
been described.
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CONT.
Observing

ventilatory frequency, use of
accessory muscles, breath sounds, and
oxygen saturations.
 Reduced respiratory effort may require
bag-valve-mask ventilation until a
definitive airway can be secured

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C: ASSESS THE CIRCULATION
In

terms of cardiovascular status (heart
rate, arterial pressure, and capillary
refill) and the effect of circulatory
inadequacy on other organs (mental
state, urine output, skin
temperature, and colour).

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CONT.
Hypotension

should initially be treated
with a 20 ml/ kg crystalloid bolus,
remembering that if it is caused by
specific toxins such as β-blockers, the
specific antidote should also be given,
for example, glucagon

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CONT.
Arrhythmias

associated with poisoning
are best treated by:
i. Correcting precipitating factors (e.g.
hyperkalaemia and acidosis)
ii. Administering the appropriate
antidote;

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CONT.
Children

in cardiac arrest should be
treated according to standard guidelines
(e.g. The Advanced Cardiac Life
Support protocol), although it is
important to address the need for a
specific antidote, for example, sodium
bicarbonate for tricyclic antidepressant
(TCA) poisoning

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SALICYLATES POISONING

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Assessment
Symptoms
Tinnitus
Seizures
Vomiting
Hyperthermia
Hyperventilation Dehydration

Lethargy
Coma

Hypoglycemia
Non cardiogenic pulmonary edema

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Cont.
•

Initial respiratory alkalosis (may be
transient), followed by paradoxical
aciduria (pH <6), then metabolic
acidosis & Hypokalemia (± ongoing
respiratory alkalosis).

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Patients Requiring Treatment
 Acute ingestion ≥ 150mg/kg
 All symptomatic patients
 Ingestion of unknown quantity

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 Investigations

Serum salicylate level at presentation (on
patients requiring treatment), and 2 hrly if
symptomatic or enteric coated preparation.
(Need to call the RCH lab to get test run
urgently as it is sent to RMH for analysis)
 Urea & electrolytes, creatinine, acid-base,
glucose


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



Management

Asymptomatic
 Charcoal 1g/kg (if <1 hour since ingestion unless
enteric coated preparation)
 Observe 6 hours & discharge if still asymptomatic
 If enteric coated preparations, serial salicylate levels
(2 hourly)
 Admit if levels have not plateaued at 6 hours post
ingestion
 I.V. bicarbonate infusion 1mmol/kg/hr to correct any
acidosis (pH <7.3)
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Cont.


Symptomatic
 All symptomatic patients require urgent medical
assessment and investigations as above.
 Charcoal 1g/kg unless altered conscious state
(protect airway first)
 I.V. fluid resuscitation to correct dehydration (use
N. Saline)

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Symptomatic (Cont.)
 I.V. bicarbonate infusion 1mmol/kg/hr, after
initial slow bolus of 2mmol/kg, (keep urine pH
>7.5)
 Potassium replacement as required
 Worsening symptoms, convulsion, coma, contact
I.C.U. for respiratory support hemodialysis
 Salicylate level >7mmol/l following an acute
poisoning contact I.C.U. for consideration of
hemodialysis.
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PARACETAMOL POISONING

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 Patients
1.
2.
3.

Requiring Management
Acute ingestion of > 200 mg/kg
Ingestion of unknown quantity
Repeated supratherapeutic ingestion of
> 100mg/kg/day

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Assessment
 Consider the possibility of co
ingestions, either accidental or deliberate

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Management
 Activated charcoal is not useful in liquid
ingestions due to rapid absorption
 Activated charcoal 1 g/kg may be considered
in a cooperative patient seen within 1 hour of
tablet or capsule ingestion.
 Serum paracetamol level at (or as soon as
possible after) 4 hours post ingestion
determines the need for N-acetyl cysteine
(NAC) administration. (see nomogram)
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 There

is no benefit in measuring
paracetamol level earlier than 4 hours
 It is safe to wait for the paracetamol level to
decide on the need for NAC in all cases that
present within 8 hours of ingestion.

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Cont.
 Patients who present > 8 hours after a toxic
ingestion / symptoms of toxicity (RUQ pain or
tenderness, nausea, vomiting) should be
commenced on NAC immediately.
 The decision to continue or cease NAC is then
based on the paracetamol level.
 Delaying NAC administration beyond 8 hours is
associated with a progressive increased risk of
liver injury.
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 There

is little evidence to guide management
in repeated supratherapeutic doses. Potential
toxicity should be assessed when:
 > 200 mg/kg (or 10g) ingested over a 24
hour period
 > 150 mg/kg/day (or 6 g) ingested over a 48
hour period
 > 100 mg/kg/day ingested over a 72 hour
period
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N- Acetyl cysteine (NAC) Infusion
Instructions
 The standard administration of NAC is a 3
stage infusion giving a total dose of 300
mg/kg:
1. 150 mg/kg over the first hour
2. 50 mg/kg over the next 4 hours
3. 100mg/kg over the next 16 hours
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Cont.
 For patients > 110 kg, calculate the dose based
on 110 kg body weight.
 NAC may be diluted in 5% dextrose or 0.9%
saline (normal saline).
 It can also be diluted in combination dextrosesaline solutions not exceeding these
concentrations including 0.45% saline in 5%
dextrose, and 0.9% saline in 5% dextrose.
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For
1.

2.

3.

adolescent / adult:
150 mg/kg in 250 or 500 ml over 1
hour
50 mg/kg in 500 ml over 4 hours
100 mg/kg in 1000 ml over 16 hours

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IRON POISONING

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IRON POISONING
Background
 Iron

is found in several different forms in
different medicines.
 The important ingestion is the amount of
elemental iron not the iron salt.

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IRON POISONING
Table: Iron Medications

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IRON POISONING
Percentage elemental iron:
• Ferrous fumarate 33%
• Ferrous chloride 28%
• Ferrous sulfate 20%
• Ferrous chloride 28%
• Ferrous gluconate 12%
Iron is also found in plant fertilizers
(e.g. sulphate of iron -20% elemental iron).
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ASSESSMENT
Patients Requiring Assessment
1. Ingestion of > 40 mg/kg elemental iron.
(approximately > ½ tablet/kg or 6.5 ml
syrup/kg)
2. Ingestion of an unknown quantity.
3. Any symptomatic patients

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HISTORY AND EXAMINATION
Initial symptoms:
 Usually occur within 20 minutes
 Nausea, vomiting, diarrhea, abdominal
pain, hypotension, Hematemesis, fever
 Gastrointestinal symptoms related to the corrosive
nature of iron may occur without systemic
toxicity, however any symptoms require iron levels.
 Lack of symptoms within the first 6 hours makes
significant toxicity unlikely.
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Latent period:
 There is often 6-24 hour latent period when
initial symptoms resolve, before overt
systemic toxicity
 Thus improvement over this time may be a
result of improvement or deterioration

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Other symptoms:
 Usually appear at 6-24 hours and last 12-24
 Tachycardia, vasoconstriction, hypotension
and shock
 Metabolic acidosis can occur.
 These are related to fluid shifts from
intravascular to extravascular compartments
and cellular hypoxia
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Multiple organ failure:
 Occurs 12-48 hours after ingestion
 Particularly hepatic failure

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IRON POISONING
Management
 ABC

 Supportive

therapy to maintain adequate
blood pressure and electrolyte balance is
essential
 I.V. fluid resuscitation 20 ml/kg
 Potassium and glucose administration as
necessary.
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IRON POISONING
Investigations
Asymptomatic patients:
 If tablet ingestion do AXR and if negative does not need further investigation or
observation
 If unknown amount or >60mg/kg ingested
need serum iron levels 4 hourly until falling
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IRON POISONING
All symptomatic patients should have the
following investigations:
 AXR if tablet ingestion
 ABG/CBG (acidosis)
 Glucose (hyperglycaemia)


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IRON POISONING
Cont.


Serum iron
 Peak levels are usually seen at 4 hours.
 Levels taken after four hours may underestimate
toxicity because the subject iron may have either been
distributed into tissues or be bound to ferritin.
 In the case of slow release or enteric coated
tablets, levels should be repeated at six to eight hours as
absorption may be erratic.
 Once desferroxamine is commenced, iron levels are not
accurate at most labs using automated methods
(including RCH)
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IRON POISONING
Cont.
 FBE (leukocytosis)
 U&E & Cr
 X-match
 Clotting (reversible early coagulopathy and late
coagulopathy secondary to hepatic injury)
 LFTs
 AXR may be helpful in evaluating gastrointestinal
decontamination after treatment if tablets have been
ingested.
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IRON POISONING
Cont.
 Decontamination
 Charcoal is of no benefit.
 Decontamination of choice is whole bowel irrigation
(WBI) with naso-gastric colonic lavage solution
30ml/kg/hr until rectal effluent clear (contraindicated if
there are signs of bowel obstruction or haemorrhage).
 WBI is indicated:
 If AXR reveals tablets, or capsules ingested
 In symptomatic patients

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IRON POISONING
Antidote:
 Desferroxamine is a chelating agent which
forms a water soluble desferroxamine-iron
complex.

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IRON POISONING
Consider desferroxamine in:
 Serum iron levels > 90 micromol/l
 Level 60 - 90 micromol/l and tablets visible on
XRay or symptomatic (nausea, vomiting, diarrhea,
abdominal pain, haematemesis, fever)
 Any patient with significant symptoms of altered
conscious state, hypotension, tachycardia,
tachypnea, or worsening symptoms irrespective of
ingested dose or serum iron level.
 Do not wait for iron level if altered conscious state,
shock, severe acidosis (pH <7.1), or worsening
symptoms but commence Desferroxamine without
delay.
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IRON POISONING
 Dose:

Desferroxamine 15 mg/kg/hr I.V. The rate
is reduced after four to six hours so that the total
intravenous dose in general does not exceed 80
mg/kg/24 hours.
 Desferroxamine -iron complex is renally excreted.
 If oliguria or anuria develop, peritoneal dialysis
or hemodialysis may become necessary to remove
ferrioxamine.
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IRON POISONING
 It

is difficult to determine the endpoint for
chelation therapy.
 Significant poisoning usually requires 12 16 hours,

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IRON POISONING
Cont.
It is recommended to continue desferroxamine
until:
 Patient is asymptomatic.
 decontamination complete
 anion-gap acidosis resolved
 Iron level (if measurable) is <54 micromol/L
 Desferroxamine has been associated with
pulmonary toxicity and should be used with
caution if indications persist >24 hours.
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HYDROCARBON POISONING

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Hydrocarbons Include:
 Petrol
 Kerosene
 Lighter Fluid
 Mineral Turpentine
 Paraffin Oil
 Lubricating Oil
 Furniture Polishes
 2 Stroke Fuel
 Diesel Fuel
 White Spirit
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Assessment
 Main complication is Aspiration Pneumonitis
 C.N.S. toxicity can be evident (either depression or
excitement)

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 Symptoms:
 Coughing,

choking, respiratory distress
ataxia, drowsiness, coma, convulsions
persistent burping (particularly seen after
petrol ingestion

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MANAGEMENT

Keep nil orally charcoal is contraindicated.
 Asymptomatic
 Observe 6hours
 Discharge if remains asymptomatic
 Arrange review by LMO the following day

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MANAGEMENT (CONT.)
 Symptomatic







If develops respiratory symptoms
(aspiration), do CXR & O2 saturation
Give O2 to maintain saturation > 94%
If stable, admit to general medical ward
If increasing O2 requirements or increased
respiratory distress contact I.C.U.
If altered conscious state at any time contact
I.C.U.
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ALKALIS POISONING

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ALKALIS POISONING

Alkalis include:
 Drain cleaners, Oven cleaners
 Automatic dish washing liquids & powders
 Laundry detergents, Ammonia
 Portland cement

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ALKALIS POISONING
 pH

of >11.5 is likely to cause significant GI
ulceration
 Attempt to obtain container to check
contents and strength of substance.

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ALKALIS POISONING(CONT.)
Corrosive potential varies with concentration of
specific ingredients and preparations, ie liquid
preparations are more likely to cause esophageal
burns than powders.
 Check preparations with Poisons Information Centre
to determine whether ingested substance is
weak, strong, irritant or corrosive in nature.


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ASSESSMENT
 Toxicity

Exposure may lead to severe burns of GIT,
especially esophagus
Absence of mouth or pharyngeal ulcers does
not preclude gastro- oesophageal lesions
 Symptoms: May be minimal
 Pain
 Nausea & vomiting, drooling or refusing to eat
and drink
 Stridor, respiratory distress
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MANAGEMENT
 Activated

charcoal is contraindicated
 If asymptomatic treat with fluid dilution:
10ml/kg of water (max 250ml)
 If asymptomatic after 4 hours and able to
eat and drink the patient can be safely
discharged
 If any symptoms, contact surgical
registrar, & admit for oesophagoscopy
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ANTICONVULSANT POISONING

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ANTICONVULSANT POISONING


CARBAMAZEPINE, PHENYTOIN, SODIUM
VALPROATE, PHENOBARBITONE

Assessment
 CNS
 Ataxia, drowsiness, coma, convulsions
 GIT
 Nausea & Vomiting
 CVS
 Hypotension, Arrhythmias
 Drug levels are available for some anticonvulsants e.g.
carbamazepine, phenytoin, phenobarbitone
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PATIENTS REQUIRING TREATMENT
 All

symptomatic patients
 Acute ingestion of unknown quantity
 Carbamazepine ingestion of >20mg/kg (for
patients not on maintenance treatment) or
the greater of more than twice the daily
dose or 20mg/kg for patients on
maintenance treatment
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MANAGEMENT
Charcoal 1g/kg unless altered conscious state (protect
airway first)
 Mild symptoms (e.g. ataxia, blurred vision)
 observe 4 hours, discharge if symptom free
 Moderate or persistent symptoms (after 4 hours of
observation)
 Admit for observation
 Severe symptoms
 Depressed conscious state or cardiac arrhythmias
contact I.C.U. .


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TRICYCLIC OVERDOSE

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TRICYCLIC OVERDOSE

Assessment
Symptoms
 Anticholinergic
 vomiting, blurred vision, ataxia, tachycardia, urinary retention
 Antiadrenergic
 vasodilatation
 Sodium Channel blockade
 widened QRS (>0.12 ms)
 QT prolongation
 reduced cardiac contractility & hypotension
 CNS Depression
 drowsiness, coma, convulsions
 Symptomatic patients require urgent medical assessment
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MANAGEMENT
Charcoal 1g/kg unless altered conscious state (protect
airway first)
 Require ECG, cardiac monitoring
 Asymptomatic: observe for 6 hours post ingestion and
discharge if have a normal ECG just prior to discharge
 All symptomatic patients should be admitted
 If widened QRS on ECG commence Sodium Bicarbonate
infusion 1mmol/kg/hr, after initial slow bolus of 2mmol/kg
 If altered conscious state, widened QRS or arrhythmia
contact I.C.U. & protect airway


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BENZODIAZEPINE POISONING

Assessment
Symptoms
 CNS depression, drowsiness, coma
 Respiratory depression
 Hypotension
 Beware additive toxicity with other CNS &
Respiratory depressants
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PATIENTS REQUIRING OBSERVATION

 Ingestion

of ≥3 times recommended dose

for age

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MANAGEMENT
 Charcoal

is not usually of benefit (due to
low order of toxicity)
 If depressed state of consciousness, protect
airway and contact ICU
 Antidote available - Flumazenil, not
indicated for ingestions and should only be
used after discussion with consultant staff.
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THEOPHYLLINE POISONING

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THEOPHYLLINE POISONING
Assessment
 CNS
 Agitation, hyperventilation, headache, convu
lsions
 Cardiovascular
 Arrhythmias
 GIT
 nausea & vomiting (may be
intractable), thirst, diarrhea
Management/
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Acute poisoning


Khorfakkan Hospital

PATIENTS REQUIRING TREATMENT

ingestion of ≥ 10mg/kg
 Any ingestion while on maintenance
theophylline
 Acute

Management/
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3

Acute poisoning


Khorfakkan Hospital

INVESTIGATIONS
Theophylline levels should be determined on all patients
requiring charcoal
 Serial levels are required at 2 hours then every 2 hours
until peak reached or decline demonstrated.
 If slow release preparation has been taken:
admit, continue levels at 4 hourly intervals after decline or
plateau to ensure detection of secondary peak
 Seizures are common at levels >330 micromol/L
 Haemoperfusion commonly needed at levels > 550
micromol/L.
 U&E, Cr and Glucose on all patients.


Management/
12/23/201
3

Acute poisoning


Khorfakkan Hospital

MANAGEMENT

Asymptomatic
 Charcoal 1g/kg
 Observe 4 hours. If no symptoms,
discharge if not slow release medication.
 If ingestion of slow release preparation,
admit for observation and serial drug
levels
Management/
12/23/201
3

Acute poisoning


Khorfakkan Hospital

MANAGEMENT(CONT.)
Symptomatic
 Charcoal 1g/kg initially unless altered conscious state
(protect airway first) then 0.5g/kg 4 hourly, and whole
bowel irrigation with colonic lavage solution 30ml/kg/hr.
 Cardiac monitoring
 I.V. fluid resuscitation & maintenance of adequate hydration
is vital
 If depressed conscious state, arrhythmias or intractable
vomiting contact I.C.U. as likely to need intubation
 Severe intoxication may require haemoperfusion
 If agitated, may need sedation with a benzodiazepine or
phenobarbitone.
Management/
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Acute poisoning


Khorfakkan Hospital

ETHANOL POISONING

Management/
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Khorfakkan Hospital

ETHANOL POISONING
Ethanol Containing Preparations














Light beer 2% Beer 5%
Cider 5%
Wine 10%
Wine coolers 5%
Fortified wine 20%
Spirits 45%
Liqueurs 30%
Perfumes& colognes >60%
Aftershaves 80%
Mouth washes (some) 25%
Methylated spirit 95% (does not contain methanol)

Management/
12/23/201
3

Acute poisoning


Khorfakkan Hospital

ETHANOL POISONING
Fatalities generally occur with blood levels > 86.8mmol/L
(breath alcohol >0.4)
Assessment
Symptoms
 Nausea, vomiting, abdominal pain
 Hypoglycemia
 Ataxia, lethargy, coma, convulsions
 Respiratory depression


Management/
12/23/201
3

Acute poisoning


Khorfakkan Hospital

ETHANOL POISONING(CONT.)
Hypothermia
 Hypokalemia, metabolic acidosis
 Unexplained drowsiness, hypothermia or hypoglycemia in
adolescents may be ethanol induced. In adolescents ethanol
ingestion often accompanies ingestion of other drugs.
Patients Requiring Treatment
 symptomatic patients


Management/
12/23/201
3

Acute poisoning


Khorfakkan Hospital

MANAGEMENT
 Charcoal

is of no benefit
 Check blood glucose in younger children
 Asymptomatic or Mild Symptoms (decreased
inhibition, slight incoordination)
 Observe for 2 hours
 Give frequent carbohydrate containing drinks
 Breath alcohol if possible
 If remains symptomatic or symptoms worsen
admit
Management/
12/23/201
3

Acute poisoning


Khorfakkan Hospital

MANAGEMENT(CONT.)
Symptomatic (more than just mild symptoms or
continued symptoms after 2 hours)
 Blood ethanol measurement, U& E, Glucose
 I.V. fluid
 Temperature regulation
 Admit.
 If unconscious or convulsions contact I.C.U.

Management/
12/23/201
3

Acute poisoning


Khorfakkan Hospital

REFERENCES
 American Association

of Poison Control Centers:
http://www.aapcc.org/dnn/Home.aspx
 American Academy of Clinical Toxicology:
http://www.clintox.org/index.cfm
 Centers for Disease Control and Prevention,
Section on Environmental health:
http://www.cdc.gov/Environmental

Management/
12/23/201
3

Acute poisoning


Khorfakkan Hospital

THANK YOU

12/23/201
3

Acute poisoning


Khorfakkan Hospital

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